Podcast 79 – Reducing Door to tPA Time in Ischemic Stroke

Another ENLS topic: Ischemic Stroke. But not the entire subject, and not even whether we should give tPA to stroke patients. Why not the latter topic–because I am not smart enough to know the answer. For that listen to David and Ashley and make your own decision. What we will talk about today is reducing door to tPA time.

There was a recently published study that gave an excellent description of one center’s interventions to get their door to tPA time down to a ridiculously low level.

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Scott Weingart. Podcast 79 – Reducing Door to tPA Time in Ischemic Stroke. EMCrit Blog. Published on August 5, 2012. Accessed on December 10th 2016. Available at [http://emcrit.org/podcasts/reducing-door-to-tpa-time/ ].

Discussion

IST-3 seemed to suggest that there may not be a direct correlation between time of thrombolytic administration and outcomes (within the 6 hour window anyway). Even if we set aside the issue of whether to “believe” in tPA at all, isn’t there still an outstanding question of whether every second matters? Or do you feel that, if we posit the first, the second is a gimme?

The problem with IST-3 is due to its methodology as an equipoise enrollment study, I can’t really do anything with the data. So for me if we believe tPA works and we believe its mechanism is similar to other conditions in which tPA works, then time definitely matters.

Interesting study. It’s a great example of using some unconventional thinking to get a result. I also like the use of the EMS transport interval to register the patient, query the family about onset time, etc. That being said…

One thought: they didn’t mention how these CVAs were confirmed. No mention of subsequent MRIs or other confirmatory tests. They mention (only in the discussion) that they had a “stroke mimic” rate of 1.4%, but do not mention how they figured this. It likely comes from a prior study of the same population (http://www.ncbi.nlm.nih.gov/pubmed/22000770) where they claimed a 1.4% mimic rate, but also noted that 28% of the treated patients had a “neuroimaging-negative ischemic stroke.” Others have discussed that study (http://www.emlitofnote.com/2011/10/third-of-tpa-patients-do-not-have.html).

Perhaps that explains why, despite this admittedly stunning reductions in DNT and OTT, the rate of good outcome at 3 months shows no trend over the years. “Time is brain” has some inherent logic to it, but it seems darn hard to demonstrate that empirically, as alluded to by Brandon.

It’s a great paper insofar as it illustrates how to perceive and overcome barriers in emergency treatment of various diseases. With regard to stroke medicine it itself, however, it doesn’t seem as illuminating.

No need for consent, it is standard of care, AAN, AHA endorse it. Consent may delay it as well. In patients without decisional capacity (aphasia, neglect, etc) or surrogate, the emergency doctrine if implied consent can be applied… Just give it if the patient meets criteria.

Fred,
Great to have you here. But that wasn’t the question at all. Agree right patient, no surrogate, pt can’t consent–give it. The question, and I’d love to hear your opinion is whether you get consent when a surrogate is there, i.e. wife is standing next to the aphasic patient. And if you do get consent, do you tell them: this medicine will help, it also has a very small risk of bleeding. Or do you tell them: this medicine has a chance of improving your neurological function in a few months, but will increase the chances of you bleeding into your head by a factor of 10.

Sorry or the confusion, wanted to add a comment on how to improve door to needle times. Waiting for consent seems to be one of those things that could potentially lead to delays. I don’t usually get consent for IV tpa , however, I inform family members of the benefits risk and potential outcome particularly if within 3-4.5 hour window. In my discussion, I use the approach by Howard et al: ” Of 100 patients treated with tissue-type plasminogen activator (tPA) instead of with placebo, 48 patients will be better with tPA, whereas 31 patients will be better with placebo. Twenty one (21) patients appear the same with either treatment.” (Stroke 2012; 43: 664-669). Even though they have a higher risk of bleeding, this doesn’t affect the otcome. The proportion of benefit is higher in stroke patients receiving TPA, but there is still a proportion of people who will do well without receiving TPA. The risk benefit analysis always favor giving TPA but patients should know what would happen if you don’t.

TPA wonder drug for stroke.Of coarse it is, when it is being endorsed by the drug company that made it.You Wouldn’t think when it comes to money any one would care for an innocent life or lives being robbed from this drug.All that studying as a Neurologist surely would open your fucken mind.No such luck!!!TPA kills.I know!!!!I saw it first hand…..

Great recommendation to follow local facility rules despite your personal beliefs of where TPA falls on the snake oil – magic bullet spectrum.

I agree that formal consent is challenging. I am working on an easy to interpret document that has neurology buy in that provides a range of potential benefit, clarifies the risk, and hopefully ensures everyone is giving the patient / relative the same numbers:
“if we gave 100 people this medicine, between 1(generous bone thrown to IST3) and 11 (NINDS/ TPA package insert) more people would be alive and independent at 6 months. 4 more people would die in the first week and regardless of getting the medicine or not 27 would be dead at six months.
In patients that don’t get the medicine 35/100 were alive and independent at 6 months (IST3)”
We shouldn’t undermine the neurologists, and they shouldn’t promise a magic recovery.

I am one of the ED pharmacists. We are included in the stroke team pages. We have a “stroke kit” with tpa, dosing calculator, all the supplies needed to mix it, an administration set, labels etc in a small tub. There are 2 of these in the ED pharmacy at all times. This can go to the bedside for preparation or be mixed in the pharmacy which is a few steps from the patient. We are proactive in finding out where we are with the patient evaluation, getting the weight and knowing exactly what bolus and infusion dose we will prepare. We also provide support when the nurses get ready to administer the tpa so they know exactly how to do it. I think the ischemic stroke kit works well for our ED Great podcast. Thanks. MaryEditors Update:
Mary posted an image of the kit

http://www.flickr.com/photos/21658512@N03/7737656362/in/photostream
This is the type of stroke kit we keep in the ED pharmacy and on the pharmacy satellites to respond to a tPA treatment request as quickly as possible. It should be tailored to each institution’s needs but this is a good example. It works really well for us.
Mary Shue, ED Pharmacist
University of Michigan Health System

The methodology discussed will GREATLY increase the number of persons getting TPA for TIA and therefore falsely improve outcomes for TPA. Further, How does one perform COMPLETE an NIH stroke scale on a CT table (ans you don’t?)

Preston–you lost me. Not sure of what is the difference between doing your exam in CT vs. a resuscitation room. Help us understand your point. I see nothing precluding me from performing NIHSS on a CT table.

Perhaps I am the one who is lost. I envisioned performing the exam with the patient supine on a narrow ct table in a relatively dark room. Visual fields would be difficult and awkward. Having the patient review the image, and reading would be awkward as as well. At the extremes points count and alter therapy. Further is seems that the more severe the stroke the more difficult it would be to perform the exam. I work in the community were at night I am the stroke team and nobody in coming. I feel that fast administration is good but rapid administration is not. I have had far to many patients return from CT already improving. The more rapid you administer this therapy the greater the likelihood that you will include patients who would have improved anyway. I must admit I am biased against this therapy. I have lost three to massive bleeds (no protocol violations…. however 2/3 had connective tissue disease Lupus and RA perhaps vasculitis risk should be considered) I believe that this therapy may work. I believe that patient selection is an issue. Thrombolytic therapy merely opens vessels. It does nothing for the ischemic penumbra. In applying the open vessel theory to the brain we don’t have a good surrogate marker for vessel occlusion. As you will recall when Thrombolytic therapy was given to patient with Unstable angina and Non ST elevation MI they actually did worse. Perhaps in the University center the protocol discussed might have some merit (with the reservations above) However, it would be difficult to apply in the community.

Our CT room is bright, not dark. In fact the lighting is better than the ED. But if you don’t like doing on the ct table, slide them back to the stretcher. If you don’t like doing the exam in the CT room, bring them back to the ED–that’s what I would do. Logistically it is difficult to tie up a CT room to save the 30 foot trip back to the ED.

While I see your point re: giving the pt time to show they are improving, we can’t just can’t wait unnecessarily. But I think in the community and most EDs, bringing the pt back to the ED makes more sense. That is why I presented the article protocol and then gave my own vision of it. I like the idea of taking the patient directly from the field to CT along with a doc and then having nursing meet us over there with an ED stretcher and a glucometer, to go back to the ED when the ct is done for the exam, etc.

I think we will have to agree to disagree on this one. I feel that the best place for examination and stabilization is the E.D. The best place to address ABC issues is in the E.D. I agree that things should be mobilized before the patients arrival. But as a practical matter….How much time is really saved in bypassing the E.D? If CT is adjacent to the ED. We are talking less than 5 minutes. If CT is far away perhaps 10-15…But if CT is that far away then valuable resources are taken from the ED to CT. Perhaps in the University setting wherein there are lots of free bodies….But in the community this is not feasible. In the protocol discussed. I do not believe that their excellent door to needle times are related to going directly to the CT suite. I believe that that their times are good because they have a dedicated team and MOST importantly a RAPID READ of the CT. All of the tasks have relatively fixed times. THE AMBULANCE BYPASSES THE RESUS BAY TO GO TO CT BAY TO CT SUITE TIME FIXED. THE TASKS WHICH WOULD BE DONE IN THE RESUS BAY ARE MERELY DONE IN CT TASKS TIME FIXED. PT GETS CT SCAN TIME FIXED. PT RETURNS TO ED TIME FIXED. In my experience the major delay is in getting the CT reading. In our shop most of the time the patient gets their CT within 20 minutes. (PARTICULARLY) After hours it is the reading which takes time. My reservation PRIMARILY is in the world in which I practice leaving the ED to be with the patient in CT leaves the ED uncovered (at times) and the advantages are unclear.I would bet you an expensive dinner if this protocol was put to a time study that the major time savings is in having a neurologist interpret the CT. In my world neurologists are not available 24/7 and on some days NOT AT ALL. BTW I simply LUV what you are doing please keep it up!

With the completion of the “Safety and efficacy of NA-1 for neuroprotection in iatrogenic stroke after endovascular aneurysm repair: a randomized controlled trial” and the success it shows in stroke after endovascular aneurysm repair. What are your thoughts on where they may go with the drug NA-1 as far as main stream stroke care?

Door to needle time.Door to needle time.I’m
Not having a stroke.I’m just wondering if anyone is taking into consideration if the the patient is a viable candidate for this drug!!And let’s make it clear door to needle time without really knowing the facts about the patient do you preform open heart surgery on a patient for just having chest pain?Do you administer TPA for mild stroke just because you have read that it’s the rite thing to do,reading all the bullshit studies on it??And then you do administer it.And as a result you go from a mild stroke to a deadly brainstem hemorrhage and I guess TPA has done it’s job.End a life and destroy a family.The motto of Do not cause harm no longer exists Neurologists may as well start calling themselves executioners aswell.

Dr. Weingart. I am an adult acute care NP with experience in critical care but am new to NCC. We respond to Code Strokes in the ER only if the patient is deemed to need ICU and frequently this is after tpa has been administered. I am having trouble with the recommendation to acutely lower BP in the setting of a suspected ischemic stroke. My understanding is that in order to improve the perfusion to the penumbra the blood pressure should not be rapidly/dramatically reduced, yet in order to infuse tpa the BP must be below 180/110. I recently watched an elderly woman’s neurological exam deteriorate in front of my eyes as her SBP dropped below 200. How do I reconcile these two conflicting recommendations?

the permissive hypertension is good for the penumbra and we shoot for up to 220 systolic for these patients. Unfortunately, in the setting of tPA, pts with hypertension will bleed at a much higher rate. So now we are balancing two risk/benefits. That pt whose neurologic exam deteriorated may have a massive post-tpa bleed if you let her bp go back up. It is tough!

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